Description
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon 5 and 4 bp deletion in exon 5
Product details:
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-BTRC, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--196°C, Appropriate long-term storage conditions--196°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Beta TRCP also known as B-TRCP Beta-TRCP or BTRC is an E3 ubiquitin ligase subunit. It has a mass of about 63 kDa and shows expression in various human tissues such as the liver brain and muscle. The BTRC domain in beta TRCP recognizes specific phosphodegron sequences in target proteins tagging them for ubiquitination and subsequent proteasomal degradation. This process helps regulate the turnover of proteins important for cell cycle progression and signal transduction.
Biological function summary
Beta TRCP participates in essential functions by being a component of the SCF (Skp1-Cullin-F-box) complex which facilitates the ubiquitination of its substrates. SCF complexes regulate various cellular processes by targeting proteins that need timely degradation. As a part of the complex beta TRCP controls the stability of pivotal substrates ensuring proper regulation of biological events like DNA replication and repair.
Pathways
Beta TRCP plays critical roles in the Wnt and NF-kB signaling pathways. These pathways depend on the precise regulation of protein levels allowing for proper cellular responses. Beta TRCP interacts with key proteins such as IkB in the NF-kB pathway and beta-catenin in the Wnt pathway controlling their ubiquitination and stability. The degradation of these proteins is necessary for pathway activation or repression influencing cell proliferation and survival decisions.
Beta TRCP has associations with cancer and inflammatory diseases. Abnormal beta TRCP function can lead to dysregulation of the NF-kB and Wnt pathways contributing to tumorigenesis and chronic inflammation. In cancers for example its relationship with proteins like beta-catenin influences tumor growth due to improper degradation. In inflammatory diseases disrupted interaction with IkB leads to excessive activation of NF-kB promoting inflammatory responses. Understanding these interactions can provide insights into therapeutic strategies.
